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* Department of Human Nutrition, The Royal Veterinary and Agricultural University, Frederiksberg, Denmark; The Danish Institute of Agricultural Sciences, Research Centre Foulum, Tjele, Denmark; ** The Biochemistry and Nutrition Group, BioCentrum-DTU, Technical University of Denmark, Lyngby, Denmark; and Department of Clinical Physiology, Frederiksberg Hospital, Frederiksberg, Denmark
2 To whom correspondence should be addressed. E-mail: mrf{at}kvl.dk.
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ABSTRACT |
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 TOP ABSTRACT SUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • conjugated linoleic acids • vaccenic acid • milk trans fatty acids • arterial health • blood pressure
The term, conjugated linoleic acids (CLA),3 is a collective term for a group of linoleic acid (18:2) isomers with conjugated double bonds, which were discovered in 1987 as an anticarcinogenic substance in beef (1). The fatty acids (FA) are found mainly in dairy products and ruminant meat; daily intake was estimated to be 160 mg (2), of which 
90% are the cis9,trans11-18:2 isomer (c9,t11-CLA) (3). VA, a milk trans fatty acid [t18:1(n-7)], was shown to be the major precursor of CLA in ruminants (4) and to increase the serum level of c9,t11-CLA in humans (5,6). Dietary VA may therefore contribute to the amount of CLA available to the human body.
CLA were found to have beneficial effects on diseases such as cancer, diabetes, and obesity in animals (7–9), and to reduce fatty streak formation (10,11) and reduce/prevent hypertension in rodents (12,13). However, the majority of human CLA studies found no effect on traditional risk markers of atherosclerosis, e.g., blood lipids and lipoproteins (14–18), whereas other markers such as blood pressure (BP) or vascular function have not been fully examined in humans. Industrially produced trans fatty acids (TFA), dominated by elaidic acid [t18:1(n-9)], are associated with CHD risk (19), but interestingly, milk-derived TFA, dominated by VA, are not. Thus, the effects of CLA and VA on atherosclerosis in humans require further evaluation.
If CLA and VA alter endothelial function in humans, the mechanism might be unrelated to blood lipids, and other markers are of interest. In this study we examined arterial elasticity (AE) as a measure of endothelium function, which is thought to be impaired as one of the first events in atherosclerosis. Our goal was to elucidate how a commercial mixture of CLA isomers and milk fat that was produced to have a high content of VA affected BP and AE. To our knowledge, no other study has examined the endothelial effects of CLA or VA in humans.
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SUBJECTS AND METHODS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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We performed a 5-wk double-blind, randomized, dietary parallel intervention study comprising 3 groups. The intervention length and number of participants was chosen according to the primary outcome variables (blood lipids, results are presented elsewhere for the groups receiving the VA- and the C-diet (20)), but are also suitable for changes in AE (21–23). The participants were stratified according to their BMI to be fed 1 of the 3 test diets. Weight, height, BP, and AE were measured and blood samples taken at the start and the end of the intervention after an overnight fast, which was necessary to standardize the conditions for the blood variables. Weight was also measured in wk 2 or 3 of the intervention.
Subjects. Young men were recruited by advertising in local newspapers and at universities near the Department. The baseline characteristics of the 60 participants chosen are presented in Table 1. Baseline characteristics did not differ among the 3 groups. All men were apparently healthy as indicated by a medical and lifestyle questionnaire. Exclusion criteria were: BMI > 30 kg/m2, smoking, hypertension, atherosclerotic disease, regular use of medication, or >10 h/wk of heavy exercise. All participants were instructed to maintain the same level of physical activity throughout the study. They all agreed to refrain from donating blood 2 mo before and during the study, and from taking dietary supplements and medication that might interfere with study measurements (acetylsalicylic acid). Habitual dietary intake was estimated by 4-d weighed food records before the intervention. Energy intake ranged from 8–18 MJ/d (mean 12.7 MJ) with 18–47% of energy (E%) from fat (mean 30 E%), 10–23% from protein (mean 13 E%) and 40–70% from carbohydrates (mean 53 E%). The 3 groups did not differ in habitual dietary intake. The protocol and aim of the study were fully explained to the participants (orally and in writing) before they gave their written informed consent. The Scientific Ethics Committee of the municipalities of Copenhagen and Frederiksberg (KF) 11-138-99 approved the research protocol.
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5E% from protein, 35E% from carbohydrates, and 60E% from fat (115 g). The latter replaced most of the subjects' habitual fat consumption. The amount of fat given to the participants was equivalent to the mean fat intake of Danish men (19–34 y) (26).
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Weighed 4-d food records. One or two weeks before and in wk 2 or 3 of the intervention, the participants' diets were assessed by 4-d weighed food records. The food records were coded and the energy intake and dietary composition were calculated using a national database (Dankost; National Food Agency). The 1st dietary records were used to guide the participants on how to change their diet to consume the test foods without increasing the total fat and energy content. The 2nd records tested adherence to the dietary advice, and if weight changes of >1 kg occurred at wk 2 or 3 of the intervention, the participants were advised to increase/decrease their energy intake.
Blood samples. After a 12-h overnight fast, venous blood was collected before the intervention period and at the end of the study. Blood for FA analysis was collected into tubes containing EDTA, which were kept on ice, and the samples were centrifuged at 4°C and 3000 x g for 15 min.
Fatty acid analysis of lipid classes and test fats. Total lipids were extracted from the blood samples according to the method of Folch et al. (27). Phospholipids and cholesterol esters were separated by TLC, using the solvent system heptane:isopropanol:acetic acid 95:5:1 (by vol). FAME were prepared from the dietary fat by transesterification with potassium hydroxide in methanol at room temperature (28). GC analyses were performed using a HP 6890 gas chromatograph (Hewlett-Packard GmbH). Identification and quantification of the FA were based on standards of FAME purchased from Nu-Chek Prep. Further details are presented elsewhere (20).
Arterial Elasticity and pulse pressure.
AE describes the artery's capacity to dilate when affected by increasing pressure, and was measured as AC in our study by a volume-oscillometric technique, Artcomp® (Criticon) described elsewhere (29,30). This method takes into account the transmural pressure (TMP, the difference between the intra- and extra-arterial pressure), at which the measurements are made (isobaric arterial compliance). This is necessary because there is a nonlinear relation between AE and TMP (31). AC is the absolute change in arterial volume (AV) for a given change in TMP (AC = 
AV/TMP). Measurements were performed on the upper left arm in a supine position after a minimum of 15 min rest at room temperature in a calm environment. AC was measured with a 10-cm wide occlusive cuff connected to a computer, which registered the volume changes concomitant with 10-mm Hg step-wise deflations from approximately –60 mmHg to +60 mm Hg TMP. The AC at higher TMP was calculated. The absolute AV was calculated from AC: AV = 
(AV/PP)TMP, where PP is the pulse pressure (PP = SBP – DBP). AD is the relative change in arterial volume for a given change in TMP and was obtained by dividing AC by AV at the same TMP: AD = AC/AV = AV/(TMP·AV). The BP was recorded by the same equipment and was used to calculate the PP. Increased PP is associated with increased risk of cardiovascular disease (32,33), and may be an indicator of stiffening of the arteries that causes raised SBP, without a simultaneous rise in DBP.
Statistics. To compare the effects of the 3 diets, a mixed model analysis of covariance was performed. The baseline values were used as covariates and the analyses were thereby adjusted for the baseline values of each variable. Fixed effects were type of diet and TMP values, and participant ID as the random factor. The SAS statistical package (version 8.2; SAS Institute) was used for all statistical analyses. When significant effects were detected (P < 0.05), the Tukey-Kramer test was used for a post hoc pair-wise comparison. When necessary, values were transformed logarithmically to normalize the distribution of residuals and to obtain variance homogeneity. Statistical tests were performed on the transformed data. Transformations were necessary for AC, AD, and AV and did not change the results. Data describing the characteristics of the participants are summarized as means ± SD, and data on outcome variables are expressed as means ± SE, adjusted for baseline values. Baseline BMI was included in the model initially because it was a stratification variable, but it had no influence on the results and was therefore removed again.
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RESULTS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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20% higher energy intake during the intervention than the control group (P = 0.004 and 0.001 respectively). However, the distributions of protein, carbohydrate, and total fat did not differ among the 3 groups. Participants fed the VA diet had a 55% higher intake of monounsaturated fatty acids (MUFA) than the control group (P < 0.0001). Participants fed the CLA diet had a 30% higher intake of PUFA than the control group (P = 0.005). Both differences corresponded to the differences in the FA composition of the test diets.
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SBP tended to be 3 mm Hg higher in the men who consumed the CLA-diet compared with the control diet (P = 0.07), but DBP or PP were not affected by the test diets Table 5.
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DISCUSSION |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The endothelium is a large endocrine organ with a central role for the development of atherosclerosis. Initial damage to the endothelium is thought to induce the inflammatory response, which may affect AE through the regulation of cytokines, adhesion molecules, and also vasoactive agents as nitric oxide. Some studies demonstrated that AE is sensitive to dietary intake even when lipoproteins are not affected (21,37,38), and AE may therefore help detect changes in CHD risk before traditional risk markers are affected. The mechanisms of CLA's actions are still uncertain, but CLA may affect endothelial function and NO production by altering the eicosanoid and cytokine production through reduced arachidonic acid availability (7,39). Another theory is that CLA affects hepatic lipid metabolism through its actions as a PPAR ligand (40). Other mechanisms have also been suggested, but they remain speculative. The effect of CLA on blood pressure is often ascribed to the concomitant effect found on adipocytokines in animal studies (12,13).
The 3 test diets did not have differential effects on any outcome variable. It is possible that there are no effects of diets rich in CLA or VA on BP or AE indices, but other possibilities are also considered here.
All participants in our study were lean young men with no hypertension or atherosclerotic disease in which improvement of any atherosclerotic variable may be difficult. It is possible that using an obese, atherosclerotic, and/or hypertensive population group would have provided different results, especially because the animal studies that noted the atherosclerosis-reducing properties of CLA all were conducted in obese, atherosclerotic, or hypertensive rodents.
Our study period was 5 wk long, and although endothelial changes may occur within this time frame (21–23), changes in plaque formation and BP are thought to occur more slowly. However, a few studies did find a small, but significant effect of dietary changes on BP after only 28–30 d (41,42). Thus, our study period may be appropriate for detecting changes in AE and BP if they are unrelated to plaque formation.
Another concern is the bioavailability of our test fats. The analysis of the FA composition in TAG, CE, and PL, which together reflect the FA eaten within our study and during the last weeks (43,44), did mirror the proportion of the fatty acids in the test diets. But were the proportion of incorporated CLA (both from the diet and from a possible bioconversion of VA to c9,t11-CLA) high enough to induce our hypothesized effects? One study reported proportions of incorporated FA in PL after CLA supplementation (14), and they found proportions of total CLA similar to ours. Because that study did find a biological (body fat–reducing) effect of the CLA supplement, the bioavailability of CLA in our study is likely to have been sufficient. The dose of CLA used in our study was similar to that used in other human CLA studies (14–16), but the amount of CLA in the animal atherosclerosis studies was typically 10 times as high or even higher; this difference cannot be ruled out as a possible explanation for the discrepancy between the results from human and animal studies.
All of our participants had a high intake of SFA from the test diet during the intervention. This may not affect BP measurements as shown by Mensink and colleagues (45), but cannot be excluded to have counteracted or drowned out the potential effect of the CLA isomers and VA on AE. In some (22,23) but not in all cases (46), diets rich in SFA were shown to have a nonbeneficial effect on AE compared with diets rich in unsaturated FA, especially MUFA.
The VA diet had a higher content of VA, c9,t11-CLA, oleic, and stearic acids, and a lower content of palmitic, myristic acids, and short-chain FA; thus we compared the effect of a diet based on milk fat high in VA, and not VA per se, with conventional milk fat. The effect of MUFA from the VA diet on AE was not apparent in this study, but the results presented elsewhere (20) showed that after the diet rich in VA, the participants had significantly lower total and HDL cholesterol levels than the control group. This affect was assigned to the difference in the content of MUFA.
One last concern may be that the men fed the control diet had a significantly lower energy intake than the other 2 groups. However, the anthropometric measures did not differ between the groups, nor did the weight change during the intervention, and the reason for the lower energy intake is therefore not clear; It is possible that underreporting may explain the disagreement.
An important aspect of this study is that the diet rich in VA, and also in other milk TFA, did not adversely affect AE or BP, and thus CHD risk. Industrialized TFA have in several studies been found to severely increase the risk of CHD (19), whereas milk TFA have not been well examined.
In conclusion, this study does not provide evidence for an effect of diets rich in a mixture of CLA or VA on blood pressure or isobaric arterial elasticity when measured in healthy young participants by a volume-oscillometric method, but may have a different effect in a more atherosclerotic population group. Future studies must elucidate how CLA isomers exert their beneficial effect on blood pressure and fatty streak formation seen in animals, and investigate whether VA may have an effect similar to CLA in humans.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: AC, arterial compliance; AD, arterial distensibility, AE, arterial elasticity; AV, arterial volume; C-diet, control diet; CE, cholesterol esters; CLA-diet, diet rich in conjugated linoleic acid; MUFA, monounsaturated fatty acids; PL, phospholipids. PP, pulse pressure; TAG, triacylglycerides; TMP, transmural pressure; VA, vaccenic acid; VA-diet, diet rich in vaccenic acid.
Manuscript received 28 September 2005. Initial review completed 4 November 2005. Revision accepted 13 January 2006.
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LITERATURE CITED |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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diet rich in conjugated linoleic acid, 
diet rich in vaccenic acid, 
control diet. Due to technical problems, 5 measurements were incomplete.